Neurogenic stunned myocardium following hemorrhagic cerebral contusion
Deleu, D.; Kettern, M-Anne.; Hanssens, Y.; Kumar, S.; Salim, K.; Miyares, F.
Saudi Medical Journal 28(2): 283-285
2007
ISSN/ISBN: 0379-5284 PMID: 17268713 Document Number: 607974
Neurogenic stunned myocardium (NSM) is a elevated serum troponin T or creatine kinase myocardial isoenzyme well-known complication of subarachnoidal (CK-MB) levels, or both, and totally reversible multifocai LVD hemorrhage, but has been reported rarely in a nonvascular pattern on echocardiography in a patient with in association with other central nervous acute severe neurologic illness without any identifiable cardiac risk system disorders. A case of NSM is factors.' Hypotension, supraventricular and ventricular arrhythmia, described in a patient with hemorrhagic reduction of cardiac output with concomitant neurogenic pulmonary brain contusion associated with cerebral edema, and exceptionally sudden death may complicate the edema. An 18-year-old man was admitted syndrome.(1) Neurogenic stunned myocardium is found in 3-5% with severe cranial trauma following a of cases with severe aneurysmal subarachnoidal hemorrhage (SAH), car roll-over. Six days after admission, he and is associated with poor clinical grade (Hunt/Hess grades III-developed findings suggestive for NSM. The V). (1,2) In addition, one study revealed that 19% of patients with acute troponin T and creatine kinase-MB level neurologic disease (hemorrhagic stroke, head injuries, and intracranial were elevated and echocardiogram showed space-occupying lesions), had increased cardiac troponin I levels apical and inferoposterior hypokinesis and indicating concomitant cardiac injury.(3) Occasionally, NSM has diffuse left ventricular akinesis with severely been reported in cerebral infarction, Guillain-Barre syndrome, reduced ejection fraction (18%). Invasive acute myelitis, and following seizures.' We describe a patient measurements confirmed low cardiac output. who developed NSM, 6 days after hemorrhagic brain contusion His cardiac function resolved completely associated with cerebral edema. within 6 days after decompressive craniotomy. This case supports the presumed unifying Case Report. An 18-year-old athletic man (professional football role of the increased intracranial pressure, player), was admitted with major cranial injuries including probably triggering a vigorous sympathetic fractures of the right temporoparietal, and base of the sphenoid bones outflow hyperactivity leading to NSM.